Experimental allergic encephalomyelitis (EAE) is a cell-mediated autoimmune neurological disease of the central nervous system characterized by delayed type hypersensitivity respose to myelin basic protein leading to inflammation and demyelination of the white matter. The experimental model disease, EAE, is similar to multiple sclerosis in man. The proposed research focuses upon the use of encephalitogenic and non-encephalitogenic peptide sequences to study effector-suppressor-cell interaction in inducing as well as in suppressing and reversing EAE. The use of various non-encephalitogenic antigens will help document specific responses bearing upon the mechanism of suppression of cell-mediated immunity and address the question of the role of encephalitogenic and non-encephalitogenic antigens in inducing and suppressing cell-mediated immunity without paralyzing the immune response to other unrelated antigens. Successful suppression and reversal of EAE with non-encephalitogenic antigens of known amino acid sequence and the elucidation of the underlying cellular mechanism for immune paralysis by specific antigens may define a rational course for treatment of similar demyelinating diseases in man.